Moderate and severe iron deficiency lowers numbers of spleen T-lymphocyte and B-lymphocyte subsets in the C57/B16 mouse

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Weanling C57/B16 mice (n=6–7) were fed diets containing 50 mg iron/kg diet (control), 16 mg iron/kg diet (moderately iron deficient) or 7 mg iron/kg diet (severely iron deficient), or were fed 50 mg iron/kg diet at the level consumed by severely iron-deficient mice (pair-fed) for 52–56 d. Spleen lymphocytes were stained with fluorescent antibodies specific for cell surface markers identifying populations of total T-lymphocytes, T-helper/inducer lymphocytes, T-suppressor/cytotoxic lymphocytes and B-lymphocytes. Cellular fluorescence was measured by flow cytometry and percentages of spleen lymphocyte populations were determined. Hemoglobin and hematocrit were highest in control mice and pair-fed mice, intermediate in moderately iron-deficient mice and lowest in severely iron-deficient mice. Liver iron level was higher in control and pair-fed mice than in moderately and severely iron-deficient mice. Percentages of spleen total T-lymphocytes and T-cytotoxic/suppressor T-lymphocytes were lowest in severely iron-deficient mice, intermediate in moderately iron-deficient mice and highest in control and pair-fed mice. The percentage of spleen T-helper/inducer lymphocytes was significantly lower in severely iron-deficient mice than in control, moderately iron-deficient and pair-fed mice. The ratio of T-helper/inducer lymphocytes to T-suppressor/cytotoxic lymphocytes was not significantly different among treatment groups. The number of spleen B-lymphocytes was lowest in severely iron-deficient mice compared to control and pair-fed mice, and intermediate in number in moderately iron-deficient mice. While distribution of spleen lymphocyte populations varied with dietary treatment, the fluoresecence properties of cells within positively stained and negative populations were not altered by iron deficiency or food restriction by pair-feeding. These data suggest that decreases in the numbers of mature lymphocytes may contribute to the impairments in cell-mediated and humoral immune functions of iron deficiency.